Table 1.

The proposed contributions of AECs to various respiratory and non-respiratory infections and diseases.

Disease	Cell	Proposed contributions to disease	Reference
COPD	Basal	Hyperplasia; smoking-induced loss of regenerative capacity and gene upregulation; increased cytokine secretion	11,20–23
	Ciliated	Reduced numbers of ciliated cells	63
	Goblet	Mucus hyperproduction; elevated SPDEF and Foxa3 expression	56
Asthma/Allergic asthma	Club	Decreased CC16 concentrations due to reduced Scgb1a1 expression	49
	Ciliated	Cdhr3 overexpression increases asthma susceptibility	59,60
	Goblet	Increased cell numbers; upregulation of proinflammatory and remodeling genes; elevated SPDEF and Foxa3 expression; MUC5AC overproduction	5,66,68,71
	PNEC	Bombesin-induced mast cell recruitment; CGRP-induced mucus secretion and ILC2 activation; γaminobutyric acid-induced goblet cell hyperplasia.	86,99,103–105
	Tuft	Express TAS2 receptors thought to attenuate allergic asthma symptoms	132–134
Cystic fibrosis	Pulmonary ionocyte	Possibly via mutation in CFTR, affecting chloride ion transport and leading to fluid accumulation in the airways, although the exact role of CFTR in ionocytes has not been described	3,4
Lung cancer	Basal	Overexpression of basal cell genes	24
	Club	Decreased serum CC16 concentrations	46
	PNEC	Source of lethal SCLC	82,111,112
	Tuft	POU2F3 expression characterizes a variant form of SCLC	147
Rhinovirus	Ciliated	High expression of Cdhr3 facilitates rhinovirus entry	58
PCD	Ciliated	Impaired cilia formation/function impedes mucociliary clearance	56
	Goblet	Aberrant mucus production	56,72
SIDS	PNEC	Hyperplasia and hypertrophy	109
Helminth infection	Tuft	Secrete IL-25 to maintain an intestinal IL-13 producing ILC2 population that stimulates tuft cell proliferation	113–115
Tuberculosis	Microfold	Facilitate Mtb binding and translocation via the B1 scavenger receptor	159,160